Interestingly, mice that are heterozygous at the Rb loci and those that have disruptions in p27Kip1 and p18Ink4c also develop pituitary tumors [88–93], and it has been shown that overexpression of the high mobility group AT-hook protein 2 (HMGA2) cooperates with loss of p27 expression or expression of CDK4R24C to promote pituitary tumor development and progression [94]. This evidence concerns the gene CDKN2C and pituitary tumor.